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Flashcards in Chest Pain and Breathlessness Deck (34)
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Name the three clinical syndromes of ischaemic heart disease

- Angina (stable and unstable)
- Myocardial infarction
- Sudden cardiac death


What can cause ischaemic heart disease

- Atheroma of coronary arteries (95% cause)
- coronary artery vasculitis (inflammation of the vessel)
- coronary artery vasospasm
- anaemia


What is the primetime for males to have there first heart attack

- Women have ischaemic heart disease later in life


What are the risk factors for ischaemic heart disease

- sex (male)
- age
- family history
- hyperlipidaemia
- hypertension
- diabetes mellitus
- smoking
- obesity
- stress
- lack of exercise


Name differences between stable and unstable angina

- comes on at rest
- unpredictable
- unstable plaque of atheroma that is changing and growing and complicating

- coronary artery disease causing the atheroma is stable
- plaque is not changing a lot
- lasts about 5-15 minutes, with exercise and emotional stress, reduces when relaxing or taking nitrates


What is the main cause of IHD

- Atheroma of coronary arteries (95% cause)


What are the theories as to how atheroma has formed

• Encrustation (Rokitansky) - platelet thrombi over injured endothelium
• Imbibition (Virchow) - low grade inflammation leads to increase plasma filtration
• Reaction to injury (Ross and Glomset) - endo injury with increase permeability and macro/smooth muscle accumulation


Describe Rokitansky theory as to how atheroma has formed

- platelets stick to the inside of the platent wall and this is due to the endothelium being injured


Describe Virchow theory as to how an atheroma has formed

- cells - low grade inflammation leads to increased plasma filtration


Describe Ross and Glomset theory as to how an atheroma has formed

- idea that there is a reaction to a vessel wall due to endothelium injury, this increases permeability and macro/smooth muscle accumulation


What part of the artery is the atheroma in

Tunica intima


Describe the pathogenesis of atherosclerosis

- At some stage there is a problem
- contents get stuck to the vascular wall
- platelets get stuck and form a thrombi
- endothelium cells either damaged directly or due to the turbulence get dislodged and expose the underlying connective tissue
- this triggers thrombosis due to the damage of the endothelium
- this triggers inflammation
- the plaques becomes more pronounced
- the smooth muscle cells migrate to the intima and become foam cells
- macrophages also take up the fat and become foam cells
- the plaque becomes bigger
- collagen is laid down
- get a plaque that is more fibrous and cellular
- the blood is still trying to get through the lumen
- get necrosis in the centre eventually
- then there is an attempt at healing and vaso vasorum grow into the intima and supply it with blood in an attempt to heal the necrosis
- dyanmic situation has occurred in the coronary artery, the plaque has ulcerated and liberated the necrotic centre and stimulated local thrombosis causing occlusion
- or the atheroma plaque has caused critical thrombi dynamic changes that cause the occlusions of the vessel


What are the complications of an atheroma

- ulceration
- fissuring
- haemorrhage
- thrombosis
- aneurysm - dilatation of a vessel (seen in an abdominal aorta due to atheroma)


What are the two main types of acute myocardial infarction

- Transmural (most cause ST elevation(STEMI))
- Subendocardial (most do not cause ST elevation (NSTEMI))


Describe a transmural actue MI

- involves the whole thickness of the ventricular wall - starts from the endocardium right through the myocardium to the epicardium


What is the most likely cause of a transmural acute MI

- underlying lesions is an atheromatous plaque in a coronary artery that has undergone fissuring and occlusive thrombosis


Describe a subendocardial infarction

- confined to the inner third or half of the myocardium - this gets in oxygen last


What is a subendocardial infarction due to

- results from generalised under-perfusion of the myocardium
- caused by generalised atheroma of all of the coronary circulation
- e.g. anaemia on top of something else
- Lung disease


If there is an occlusion of
- Main left coronary artery
- Left anterior descending
- Left circumflex
- Right coronary artery

What part of the heart does it affect?

- Main left coronary artery = massive anterolateral MI
- Left anterior descending = anteroseptal MI
- Left circumflex = lateral MI
- Right coronary artery = Posterior (inferior) MI


Describe the macroscopic appearance of the MI
- 0-12 hours
- 12-24 hours
- 24-72 hours
- 3-10 days
- weeks - months

- 0-12 hours = no changes
- 12-24 hours = pale with blotchy discolouration
- 24-72 hours = soft, pale and yellow
- 3-10 days = soft, yellow-brown with hyperaemic border
- weeks - months = white fibrous scar


Describe the histology appearance of the MI
- 0-12 hours
- 12-24 hours
- 24-72 hours
- 3-10 days
- weeks - months

- 0-12 hours = No changes
- 12-24 hours = bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis; intracellular oedema
- 24-72 hours = coagulative necrosis with loss of nuclei and striations, beginning of acute inflammatory response with heavy interstitial neutrophil infiltrate
- 3-10 days = replacement of infarcted area by granulation tissue
- weeks - months = collagenous scar tissue


How does a pathologist diagnose cardiac death due to MI after death

Cut along the coronary artery and find the infract


What are the short term complications of MI

 left ventricular failure
 cardiac dysrhythmias
 rupture of ventricular wall - blood will just go left to right
 papillary muscle infarction - can cause mitral regurgitation
 mural thrombus - if it embolisms it can convert to stroke
 fibrinous pericarditis
 deep vein thrombosis


What are the long term complications of MI

 intractable left ventricular failure
 ventricular aneurysm - thin wall where the scar is
 Dressler's syndrome
 recurrent myocardial infarction


What do the effects of a pulmonary embolus depend on

- Size of the occluded vessel
- number of the emboli
- adequacy of the bronchial blood supply


what does a saddle embolus do

- this is when it blocks both pulmonary arteries
- this can lead to circulatory collapse


Where can the PE get stuck

- large embolus coils within one major pulmonary artery
- saddle embolus - blocks both pulmonary arteries


duel blood supply....

protects lungs from effects of pulmonary artery obstruction


How does Dressler's syndrome present (long term complication of MI)

fever, pleuritic pain, pericardial effusion and raised ESR – type of pericarditis thus treated with NSAIDs


How does ventricular aneurysm present (long term complication of MI)

persistent ST elevation and left ventricular failure